PHPT1 Antibody
- Known as:
- PHPT1 Antibody
- Catalog number:
- 32170
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PHPT1 Antibody
Related genes to: PHPT1 Antibody
- Gene:
- PHPT1 NIH gene
- Name:
- phosphohistidine phosphatase 1
- Previous symbol:
- -
- Synonyms:
- PHP14, HSPC141, CGI-202, DKFZp564M173, bA216L13.10
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-23
- Date modifiied:
- 2016-10-20
Related products to: PHPT1 Antibody
Related articles to: PHPT1 Antibody
- The JAK/STAT signaling pathway is a highly conserved regulator essential for animal development. Here, we show that the phosphohistidine phosphatase 1, PHPT1/Ocnus, is required for cell survival by regulating JAK/STAT signaling. Knockdown of () leads to apoptosis of germ cells during the transit-amplifying divisions of spermatogonia in the second instar larvae. In S2 cells, overexpression reduces phosphorylated STAT (pSTAT) levels, limits its nuclear accumulation, and alters the expression of STAT target genes. Mechanistically, Ocn directly dephosphorylates Stat92E at the conserved tyrosine residue Y711. Consistently, genetic inhibition of JAK/STAT signaling via Socs36E overexpression partially rescues male sterility caused by knockdown. Moreover, human PHPT1 suppresses nuclear accumulation of pSTAT in HeLa cells, indicating evolutionary conservation. Together, our findings identify PHPT1/Ocnus as a conserved negative regulator of JAK/STAT signaling and may provide a potential target for therapeutic intervention in the treatment of STAT-related diseases, including cancer. - Source: PubMed
Publication date: 2026/09/17
Wang QianRen YueChen Meng-YanMao BinGuo XuanWan JianLiu KeTong Jing-JingWang Yu-Feng - This study aimed to comprehensively investigate the molecular mechanisms of clear cell renal cell carcinoma (ccRCC), identify key cellular subpopulations and genes, develop an effective diagnostic model, and screen potential targeted therapies for ccRCC. We analyzed single-cell transcriptomic sequencing data to identify the major cellular subpopulations in ccRCC. High-dimensional weighted gene co-expression network analysis and multiple machine learning algorithms were used to identify key genes and develop a diagnostic model. Two-sample Mendelian randomization analysis was performed to assess causality. Molecular docking was used to identify a candidate therapeutic agent. Data processing was conducted using R and Python. The proportion of endothelial cells was significantly higher in ccRCC (P < .001). High-dimensional weighted gene co-expression network analysis showed that the pink module was closely associated with endothelial cells. Univariate logistic regression and Least Absolute Shrinkage and Selection Operator identified 11 key genes: WDR83OS, TMA7, PFDN5, DSTN, PHPT1, HMGN3, TMSB10, RPL27A, RPL23A, RPL15, and RPL27. Based on these genes, a diagnostic model for ccRCC was developed using multiple machine learning algorithms and achieved an area under the receiver operating characteristic curve of 0.960. In addition, 2-sample Mendelian randomization analysis supported a causal association between WDR83OS and ccRCC (inverse-variance weighted: odds ratio = 1.160, P = .033). Molecular docking indicated that oxyphenbutazone had a high binding affinity for WDR83OS, with a binding energy of -7.124 kcal/mol. By integrating multiple bioinformatic approaches, this study identified key cellular populations and genes in ccRCC, developed a reliable diagnostic model, and highlighted WDR83OS as a potentially important therapeutic target. - Source: PubMed
Xiao LetingYusan AimureguliCao YongdeYue FangqianFeng JiaxinWu HuayanSun LinglingQiu JunboXiao YinhaoZhang Shilin - Blood is the standard matrix for gene expression (GE)-based biodosimetry, but less invasive sampling methods are needed in emergency settings and for longitudinal monitoring. Saliva, which contains leukocytes and an ultrafiltrate of blood, is a promising alternative. In this human in vivo study, we analyzed radiation-induced shifts in salivary gene expression for biodosimetric applications and evaluated their similarity to gene expression patterns in blood. Beyond dose estimation, such saliva-based gene expression signatures may support risk stratification and early prediction of clinical outcomes, particularly when repeated sampling is required or blood collection is not feasible. Matched blood and saliva samples were collected from leukemia patients (n = 31) undergoing fractionated total-body irradiation (TBI) for their myeloablative treatment (1.5-4 Gy total dose, 1.5-2 Gy per fraction). Samples were taken before and 24 h after the first day of radiation treatment. The expression of radiation-responsive genes (GADD45A, CCNG1, CDKN1A, PHPT1, SESN1, FDXR, DDB2, POU2AF1, and WNT3) was analyzed for 28 patients (three patients excluded) using quantitative real-time PCR (RT-qPCR). Significant upregulation was observed for GADD45A (median fold change = 1.52, P = 0.003), CCNG1 (median fold change = 1.73; P = 0.003), and DDB2 (median fold change = 1.60; P = 0.05), as well as WNT3 (median fold change = 1.84; P = 0.038), demonstrating that saliva shows molecular responses to radiation exposure. Notably, 54% of the patients exhibited radiation-responsive upregulation of GADD45A and CCNG1, indicating that saliva can detect radiation-responsive gene expression despite substantial inter-individual variability. Corresponding blood samples were obtained from 16 patients. Statistically significant upregulation of multiple radiation-responsive genes was observed: GADD45A (median fold change = 2.25; P < 0.001), CCNG1 (median fold change = 1.64; P = 0.010), DDB2 (median fold change = 1.91; P < 0.001), CDKN1A (median fold change = 2.45; P = 0.001), SESN1 (median fold change = 1.75; P < 0.001), and FDXR (median fold change = 2.53; P = 0.001). A significant downregulation was observed for POU2AF1 (median fold change = 0.49; P = 0.013). In conclusion, detection of radiation-induced gene expression changes in saliva may serve as a minimally invasive tool for biodosimetry. However, given the greater inter-individual variability observed in saliva compared to blood, further optimization and validation is essential before clinical implementation. - Source: PubMed
Publication date: 2026/06/03
Fischer SKasper MStewart SSchmid NO'Brien GZahradníček OMilanová MŠt'astná M MarkováSirak IMuhtadi RBadie CEder SPort MTichý AOstheim P - The ability to assign amino acid resonances in multidimensional NMR spectra of biomolecules is necessary for detailed studies of protein structure and dynamics. Despite creative advances in isotopic labeling, unlabeling and multidimensional NMR experiments, resonance assignment remains a bottleneck in studies of large proteins. In this work, we show that the metabolic flux through biosynthetic pathways of amino acid production during protein expression can be modulated to aid in the identification of resonances in two-dimensional NMR spectra. This straightforward method involves doping N-enriched minimal media with small amounts of rich natural abundance media to generate unique peak intensity attenuation patterns, producing type-specific signatures of amino acids in two-dimensional N HSQC experiments. Using three model proteins, IGPS (51 kDa heterodimer), PTP1B (35 kDa), PHPT1 (14 kDa), we show that this method can disentangle several amino acid types, is robust to different expression conditions, and is a useful supplement for triple resonance experiments in protein backbone resonance assignments. - Source: PubMed
Publication date: 2026/05/01
Cui Danica SAnderson Evan OZavala ErikLisi George PLoria J Patrick - The human protein histidine phosphatase PHPT1 is involved in several important cellular pathways and has been implicated in various cancers. However, the biological roles of this enzyme are not well understood due to a lack of chemical tools that enable its study. Herein we have identified phenylarsonic acids as general scaffolds which inhibit PHPT1 activity. Notably, phenylarsonic acids can be embedded into peptide sequences, providing the first known peptide-based inhibitors of PHPT1. In a counterscreen against a small panel of phosphatases, we demonstrate that these compounds exhibit some selectivity for PHPT1. Moreover, we show that these compounds exhibit mixed inhibition. We provide evidence that reduction of the phenylarsonic acids by reducing agents like dithiothreitol (DTT) to provide phenylarsine species gives rise to the observed PHPT1 inhibition. These As(III) species are known to be thiophilic and can interact with solvent-exposed cysteine residues of proteins. Finally, we demonstrate that mutating the three cysteine residues of PHPT1 to alanine results in a significant decrease in enzyme inhibition by the phenylarsonic acids, suggesting that these compounds likely interact at least in part with Cys residues in PHPT1. - Source: PubMed
Publication date: 2026/03/10
Keyes E DallesHollow Sophia EOblad PaulJohnstone Timothy CBarrios Amy M